Biomedicine & Pharmacotherapy,
Journal Year:
2023,
Volume and Issue:
158, P. 114168 - 114168
Published: Jan. 3, 2023
The
categorization
of
cancers
demonstrates
that
prostate
cancer
is
the
most
common
malignancy
in
men
and
it
causes
high
death
annually.
Prostate
patients
are
diagnosed
mainly
via
biomarkers
such
as
PSA
test
show
poor
prognosis.
cells
rapidly
diffuse
into
different
parts
body
their
metastasis
also
a
reason
for
death.
Current
therapies
include
chemotherapy,
surgery
radiotherapy
well
targeted
therapy.
progression
regulated
by
factors
STAT3
signaling
among
them.
Growth
cytokines
IL-6
can
induce
shows
carcinogenic
impact.
Activation
occurs
promotes
malignant
behavior
tumor
cells.
Induction
increases
glycolysis
proliferation
prevents
apoptosis.
Furthermore,
induces
EMT
mechanism
increasing
metastasis.
stimulates
drug
resistance
limitation
current
works
lack
experiment
related
to
role
radio-resistance
tumor.
Calcitriol,
capsazepine
β-elemonic
compounds
capable
targeting
its
inhibition
In
addition
natural
products,
small
molecules
have
been
developed
Signal Transduction and Targeted Therapy,
Journal Year:
2021,
Volume and Issue:
6(1)
Published: Nov. 26, 2021
Abstract
The
Janus
kinase/signal
transducer
and
activator
of
transcription
(JAK/STAT)
signaling
pathway
was
discovered
more
than
a
quarter-century
ago.
As
fulcrum
many
vital
cellular
processes,
the
JAK/STAT
constitutes
rapid
membrane-to-nucleus
module
induces
expression
various
critical
mediators
cancer
inflammation.
Growing
evidence
suggests
that
dysregulation
is
associated
with
cancers
autoimmune
diseases.
In
this
review,
we
discuss
current
knowledge
about
composition,
activation,
regulation
pathway.
Moreover,
highlight
role
its
inhibitors
in
Journal of Hematology & Oncology,
Journal Year:
2022,
Volume and Issue:
15(1)
Published: June 28, 2022
Abstract
Cancer
is
one
of
the
leading
causes
death
worldwide,
and
factors
responsible
for
its
progression
need
to
be
elucidated.
Exosomes
are
structures
with
an
average
size
100
nm
that
can
transport
proteins,
lipids,
nucleic
acids.
This
review
focuses
on
role
exosomes
in
cancer
therapy.
We
discuss
how
able
modulate
components
tumor
microenvironment
influence
proliferation
migration
rates
cells.
also
highlight
that,
depending
their
cargo,
suppress
or
promote
cell
enhance
reduce
response
radio-
chemo-therapies.
In
addition,
we
describe
trigger
chronic
inflammation
lead
immune
evasion
by
focusing
ability
transfer
non-coding
RNAs
between
cells
other
molecular
signaling
pathways
such
as
PTEN
PI3K/Akt
cancer.
Subsequently,
use
carriers
anti-tumor
agents
genetic
tools
control
progression.
then
tumor-derived
carcinogenesis.
Finally,
devote
a
section
study
diagnostic
prognostic
clinical
courses
important
treatment
patients.
provides
comprehensive
understanding
therapy,
therapeutic
value
remodeling
microenvironment.
Graphical
Biomedicine & Pharmacotherapy,
Journal Year:
2021,
Volume and Issue:
141, P. 111824 - 111824
Published: June 25, 2021
Epithelial-to-mesenchymal
transition
(EMT)
mechanism
is
responsible
for
metastasis
and
migration
of
cancer
cells
to
neighboring
tissues.
Morphologically,
epithelial
are
transformed
mesenchymal
cells,
at
molecular
level,
E-cadherin
undergoes
down-regulation,
while
an
increase
occurs
in
N-cadherin
vimentin
levels.
Increasing
evidence
demonstrates
role
EMT
mediating
drug
resistance
cells.
On
the
other
hand,
paclitaxel
(PTX)
docetaxel
(DTX)
two
chemotherapeutic
agents
belonging
taxene
family,
capable
inducing
cell
cycle
arrest
via
preventing
microtubule
depolymerization.
Aggressive
behavior
resulted
from
EMT-mediated
can
lead
PTX
DTX
resistance.
Upstream
mediators
such
as
ZEB1/2,
TGF-β,
microRNAs,
so
on
involved
regulating
response
DTX.
Tumor-suppressing
factors
inhibit
promote
sensitivity
Furthermore,
three
different
strategies
including
using
anti-tumor
compounds,
gene
therapy
delivery
systems
have
been
developed
suppressing
EMT,
enhancing
cytotoxicity
against
that
mechanistically
discussed
current
review.
Journal of Cellular Physiology,
Journal Year:
2022,
Volume and Issue:
237(7), P. 2770 - 2795
Published: May 13, 2022
Metastasis
of
tumor
cells
is
a
complex
challenge
and
significantly
diminishes
the
overall
survival
prognosis
cancer
patients.
The
epithelial-to-mesenchymal
transition
(EMT)
well-known
mechanism
responsible
for
invasiveness
cells.
A
number
molecular
pathways
can
regulate
EMT
in
nuclear
factor-kappaB
(NF-κB)
one
them.
translocation
NF-κB
p65
induce
transcription
several
genes
involved
induction.
present
review
describes
interaction
their
association
progression.
Due
to
oncogenic
role
signaling,
its
activation
enhances
metastasis
via
This
has
been
confirmed
various
cancers
including
brain,
breast,
lung
gastric
cancers,
among
others.
ZEB1/2,
transforming
growth
factor-β,
Slug
as
inducers
undergo
upregulation
by
promote
After
induction
driven
NF-κB,
significant
decrease
occurs
E-cadherin
levels,
while
N-cadherin
vimentin
levels
an
increase.
noncoding
RNAs
potentially
also
function
upstream
mediators
modulate
NF-κB/EMT
axis
cancers.
Moreover,
mediating
drug
resistance
Thus,
suppressing
sensitivity
chemotherapeutic
agents.
Carbohydrate Polymers,
Journal Year:
2021,
Volume and Issue:
272, P. 118491 - 118491
Published: July 27, 2021
An
important
motivation
for
the
use
of
nanomaterials
and
nanoarchitectures
in
cancer
therapy
emanates
from
widespread
emergence
drug
resistance.
Although
doxorubicin
(DOX)
induces
cell
cycle
arrest
DNA
damage
by
suppressing
topoisomerase
activity,
resistance
to
DOX
has
severely
restricted
its
anti-cancer
potential.
Hyaluronic
acid
(HA)
been
extensively
utilized
synthesizing
nanoparticles
as
it
interacts
with
CD44
expressed
on
surface
cells.
Cancer
cells
can
take
up
HA-modified
through
receptor-mediated
endocytosis.
Various
types
nanostructures
such
carbon
nanomaterials,
lipid
polymeric
nanocarriers
have
modified
HA
enhance
delivery
acid-based
advanced
materials
provide
a
platform
co-delivery
genes
drugs
along
efficacy
overcome
chemoresistance.
In
present
review,
potential
methods
application
are
discussed.
Journal of Experimental & Clinical Cancer Research,
Journal Year:
2022,
Volume and Issue:
41(1)
Published: July 1, 2022
Abstract
Background
One
of
the
most
malignant
tumors
in
men
is
prostate
cancer
that
still
incurable
due
to
its
heterogenous
and
progressive
natures.
Genetic
epigenetic
changes
play
significant
roles
development.
The
RNA
molecules
with
more
than
200
nucleotides
length
are
known
as
lncRNAs
these
factors
do
not
encode
protein.
They
regulate
gene
expression
at
transcriptional,
post-transcriptional
levels.
LncRNAs
vital
biological
functions
cells
pathological
events,
hence
their
undergoes
dysregulation.
Aim
review
role
alterations
development
emphasized
here.
Therefore,
were
chosen
for
this
purpose
level
interaction
other
signaling
networks
progression
examined.
Key
scientific
concepts
aberrant
has
been
well-documented
rate
tumor
regulated
via
affecting
STAT3,
NF-κB,
Wnt,
PI3K/Akt
PTEN,
among
molecular
pathways.
Furthermore,
radio-resistance
chemo-resistance
features
cells.
Overexpression
tumor-promoting
such
HOXD-AS1
CCAT1
can
result
drug
resistance.
Besides,
induce
immune
evasion
upregulating
PD-1.
Pharmacological
compounds
quercetin
curcumin
have
applied
targeting
lncRNAs.
siRNA
tool
reduce
thereby
suppressing
progression.
Prognosis
diagnosis
clinical
course
be
evaluated
by
exosomal
lncRNA-p21
investigated
serum
patients
a
reliable
biomarker.
Cancers,
Journal Year:
2021,
Volume and Issue:
13(8), P. 1882 - 1882
Published: April 14, 2021
In
cancer
cells,
a
vital
cellular
process
during
metastasis
is
the
transformation
of
epithelial
cells
towards
motile
mesenchymal
called
to
transition
(EMT).
The
cytoskeleton
an
active
network
three
intracellular
filaments:
actin
cytoskeleton,
microtubules,
and
intermediate
filaments.
These
filaments
play
central
role
in
structural
design
cell
behavior
are
necessary
for
EMT.
During
EMT,
undergo
as
manifested
by
elongation,
migration,
invasion,
coordinated
reorganization.
extremely
dynamic
structure,
controlled
balance
assembly
disassembly
Actin-binding
proteins
regulate
polymerization
depolymerization.
Microtubule
reorganization
also
plays
important
migration
polarization.
Intermediate
rearranged,
switching
vimentin-rich
network,
this
protein
used
marker
cell.
Hence,
targeting
EMT
regulating
activities
their
key
components
may
be
potential
solution
metastasis.
This
review
summarizes
research
done
on
physiological
functions
its
process,
effect
multidrug-resistant
(MDR)
cells—highlight
some
future
perspectives
therapy
cytoskeleton.
Medicinal Research Reviews,
Journal Year:
2023,
Volume and Issue:
43(4), P. 1141 - 1200
Published: March 17, 2023
Abstract
Epithelial‐mesenchymal
transition
(EMT)
is
a
complex
process
with
primordial
role
in
cellular
transformation
whereby
an
epithelial
cell
transforms
and
acquires
mesenchymal
phenotype.
This
plays
pivotal
tumor
progression
self‐renewal,
exacerbates
resistance
to
apoptosis
chemotherapy.
EMT
can
be
initiated
promoted
by
deregulated
oncogenic
signaling
pathways,
hypoxia,
cells
the
microenvironment,
resulting
loss‐of‐epithelial
polarity,
cell–cell
adhesion,
enhanced
invasive/migratory
properties.
Numerous
transcriptional
regulators,
such
as
Snail,
Slug,
Twist,
ZEB1/ZEB2
induce
through
downregulation
of
markers
gain‐of‐expression
markers.
Additionally,
cascades
Wnt/β‐catenin,
Notch,
Sonic
hedgehog,
nuclear
factor
kappa
B,
receptor
tyrosine
kinases,
PI3K/AKT/mTOR,
Hippo,
transforming
growth
factor‐β
pathways
regulate
whereas
they
are
often
cancers
leading
aberrant
EMT.
Furthermore,
noncoding
RNAs,
tumor‐derived
exosomes,
epigenetic
alterations
also
involved
modulation
Therefore,
regulation
vital
strategy
control
aggressive
metastatic
characteristics
cells.
Despite
vast
amount
preclinical
data
on
cancer
progression,
there
lack
clinical
translation
at
therapeutic
level.
In
this
review,
we
have
discussed
thoroughly
aforementioned
transcription
factors,
RNAs
(microRNAs,
long
RNA,
circular
RNA),
modifications,
exosomes
cancers.
We
emphasized
contribution
drug
possible
interventions
using
plant‐derived
natural
products,
their
semi‐synthetic
derivatives,
nano‐formulations
that
described
promising
blockers.
